Correlations of changes in inflammatory factors, glucose and lipid metabolism indicators and adiponectin with alterations in intestinal flora in rats with coronary heart disease.

OBJECTIVE: The aim of this study was to explore the correlations of changes in inflammatory factors, glucose and lipid metabolism indicators and adiponectin with alterations in intestinal flora in rats with coronary heart disease. MATERIALS AND METHODS: A total of 30 male specific pathogen-free rats were randomly assigned into two groups, including: blank group (n=15) and coronary heart disease group (n=15). The rats in the coronary heart disease group were given high-fat diets and pituitrin to establish the model of coronary heart disease. Meanwhile, rats in the blank group were administered with an equal volume of double-distilled water. The alterations in the intestinal flora of rats were detected in the two groups, respectively. In addition, the changes in the levels of inflammatory factors, glucose and lipid metabolism indicators, adiponectin, creatine kinase (CK) and its isoenzyme, as well as troponin, were also examined. RESULTS: Statistically, significant differences in the levels of glucose and lipid metabolism indicators low-density lipoprotein (LDL) (p=0.040), total cholesterol (TC) (p=0.039), high-density lipoprotein (HDL) (p=0.044), triglyceride (TG) (p=0.000) and blood glucose (p=0.046) were observed between the rats in the coronary heart disease group and blank group. The content of all the glucose and lipid metabolism indicators (except HDL) in coronary heart disease group was significantly higher than the blank group (p<0.05). The rats in the coronary heart disease group had evidently higher levels of CK (p=0.000) and its isoenzyme (p=0.019), as well as troponin (p=0.021), than those in the blank group. The level of serum adiponectin in rats in coronary heart disease group was distinctly lower than that in the blank group, showing statistically significant differences (p<0.05). Besides, the levels of the inflammatory factors interleukin (IL)-2 (p=0.011), transforming growth factor (TGF)-ß (p=0.048), tumor necrosis factor-α (TNF-α) (p=0.025) and IL-6 (p=0.038) in rats in the coronary heart disease group were dramatically higher than those in blank group. Rats in coronary heart disease group had remarkably more Actinobacteria, Desulfovibrio, Aristipus and Escherichia coli in the intestine. Meanwhile, the abundance of Flavobacterium, Burkhofer and some probiotics increased significantly in the intestine of rats in blank group (p<0.05). The changes in the abundance of Actinobacteria, Desulfovibrio, Aristipus and Escherichia coli in the intestine of rats were probably correlated with increased levels of glucose and lipid metabolism indicators, inflammatory factors and adiponectin in coronary heart disease group. Moreover, the abundance of intestinal probiotics such as Bifidobacterium and Lactobacillus in rats in coronary heart disease group was notably lower than that in blank group (p<0.05). The decline in the abundance of such intestinal probiotics as Bifidobacterium and Lactobacillus was correlated with the changes in the levels of glucose and lipid metabolism indicators, inflammatory factors and adiponectin. In addition, decreased levels of probiotics weakened normal physiological functions of the intestine and promoted disease progression. CONCLUSIONS: Inflammatory factors, glucose and lipid metabolism indicators and adiponectin have evident changes in rats with coronary heart disease, which may be correlated with the alterations in the intestinal flora.

Determination of the Role of Fusobacterium Nucleatum in the Pathogenesis in and Out the Mouth.

INTRODUCTION: One of the most important types of microorganisms in the oral cavity in both healthy and non-healthy individuals is Fusobacterium nucleatum. Although present as a normal resident in the oral cavity, this Gram-negative pathogen is dominant in periodontal disease and it is involved in many invasive infections in the population, acute and chronic inflammatory conditions, as well as many adverse events with a fatal outcome. AIM: To determine the role of F. nucleatum in the development of polymicrobial biofilms thus pathogenic changes in and out of the oral media. MATERIAL AND METHOD: A systematic review of the literature concerning the determination and role of F. nucleatum through available clinical trials, literature reviews, original research and articles published electronically at Pub Med and Google Scholar. CONCLUSION: The presence of Fusobacterium nucleatum is commonly associated with the health status of individuals. These anaerobic bacteria plays a key role in oral pathological conditions and has been detected in many systemic disorders causing complex pathogenethic changes probably due to binding ability to various cells thus several virulence mechanisms. Most common diseases and conditions in the oral cavity associated with F.nucleatum are gingivitis (G), chronic periodontitis (CH), aggressive periodontitis (AgP), endo-periodental infections (E-P), chronic apical periodontitis (PCHA). The bacterium has been identified and detected in many systemic disorders such as coronary heart disease (CVD) pathological pregnancy (P); polycystic ovary syndrome (PCOS), high-risk pregnancy (HRP), colorectal cancer (CRC); pre-eclampsia (PE); rheumatoid arthritis (RA); osteoarthritis (OA).

Cardiac emergencies: infective endocarditis, pericarditis, and myocarditis.

Cardiac infections presenting as emergencies include complications of infective endocarditis, including congestive heart failure, chordae tendinae rupture, cardiac arrhythmias, and embolic phenomenon; acute pericarditis, including cardiac tamponade; and acute myocarditis presenting with malignant cardiac arrhythmias or congestive heart failure. Most of these emergent infectious disease manifestations of the cardiovascular system have a good prognosis if diagnosed early and managed appropriately. Newer diagnostic modalities and combined treatment guidelines are available from the European Society of Cardiology and the American Heart Association.

Prediagnostic plasma antibody levels to periodontopathic bacteria and risk of coronary heart disease.

Many epidemiological studies have indicated that periodontitis is an important risk factor for coronary heart disease (CHD). We examined whether plasma antibody levels to 3 major periodontal pathogens, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia predicted the risk of CHD events. A nested case-control research design (case: n = 191, control: n = 382), by matching gender, age, study area, date of blood collection, and time since last meal at blood collection, was employed in a large cohort of Japanese community residents.Antibody levels of periodontopathic bacteria were associated with risk of CHD after adjusting for BMI, smoking status, alcohol intake, history of hypertension, history of diabetes mellitus, exercise during leisure time, and perceived mental stress. The association was different by age subgroup. For subjects aged 40-55 years, the medium (31.7-184.9 U/mL) or high tertile plasma antibody level (> 184.9 U/mL) of A. actinomycetemcomitans showed higher risk of CHD (medium: OR = 3.72; 95% CI = 1.20-11.56, high: OR = 4.64; 95% CI = 1.52-14.18) than the low tertile level (< 31.7 U/mL). The ORs of CHD incidence became higher with an increase in IgG level of A. actinomycetemcomitans (P for trend = 0.007). For subjects aged 56-69 years, the high tertile level (> 414.1 U/mL) of P. intermedia was associated with higher risk of CHD (OR = 2.65; 95% CI = 1.18-5.94) in a dose-response fashion (P for trend = 0.007). The possible role of periodontopathic bacteria as a risk factor for CHD incidence was suggested by the results of this study by the elevated antibody level to these bacteria with the increased risk of CHD.

Molecular survey of atheromatous plaques for the presence of DNA from periodontal bacterial pathogens, archaea and fungi.

BACKGROUND AND OBJECTIVE: Chronic infections, such as periodontitis, have been associated with the development and progression of atherosclerosis. The mechanisms through which this occurs have yet to be elucidated. This study was carried out to detect periodontopathic bacteria as well as archaea and fungi in atheromatous plaques and search for factors associated with their occurrence in atheromas. MATERIAL AND METHODS: A cross-sectional study was carried out including 30 patients diagnosed with atherosclerosis in the carotid, coronary or femoral arteries. Plaques were collected during surgery and analysed using PCR to detect Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola and members of the Synergistetes group. Samples were also surveyed with universal primers for bacterial, archaeal and fungal DNA. Patients responded to a questionnaire to determine factors associated with PCR results. RESULTS: All dentate individuals (66.7%) had periodontal disease, 95% of which was severe and 65% extensive. None of the targeted periodontopathic bacteria was found in the atheromas. No sample yielded positive results for fungal and archaeal DNA. Four samples (13%) were positive for the presence of bacterial DNA. Of these, three participants were dentate (two with severely chronic generalized periodontitis and one with severely chronic localized periodontitis). CONCLUSION: This study did not confirm previous findings of periodontal pathogens in atheromas, making it impossible to establish factors associated with their presence in plaques. Presence of bacterial DNA in some samples indicates that periodontal or nonoral bacterial species other than the ones targeted in this study may be involved with some cases of atherosclerosis.

Detection of Chlamydophila pneumoniae (Chlamydia pneumoniae) in endarteroctomy specimens of coronary heart diseases patients.

BACKGROUND & OBJECTIVE: Association of Chlamydia pneumoniae with atherosclerosis and coronary artery disease is debated. Increased antibody levels against C. pneumoniae in patients with coronary artery disease is widely reported. Direct evidence would be demonstration of C. pneumoniae, its antigen or genome in the diseased arterial tissue. This study was thus conducted to look for antigen or genome of C. pneumoniae in coronary artery specimens from patients with coronary artery disease along with serology. METHODS: Sixty two end arteriotomy specimens of discarded coronary arteries from patients of coronary heart disease were tested for presence of C.pnuemoniae genome using 2 nested PCR assays and antigen detection by immuno-fluorescence assay. Presence of species specific antibodies were also tested in the patients. RESULTS: C. pneumoniae could not be detected by PCR or immunofluorescence assay in any specimen. C. pnuemoniae Ig G antibody was detected in 42 of the 62 (67.7%) patients studied, compared to 10 of the 23 (43.47%) of controls. Moreover 18 of 62 (29%) patients compared to 4 of 23 (17.39%) controls possessed IgA antibodies. INTERPRETATION & CONCLUSION: Association of C.pneumoniae and coronary artery disease would not be established by genome or antigen detection. However, C. pneumoniae antibodies were detected in more number of patients than controls. More studies are required to reach to a conclusion.

Helicobacter pylori infection and coronary artery disease.

The aim of this investigation was to determine the seroprevalence of H. pylori in patients with coronary artery disease (CAD). Patients with coronary artery disease (n = 90) and control group (n = 90) were enrolled into this randomized, multi-centre study. CAD risk factors analyzed included age, male gender, diabetes mellitus, systemic hypertension, cigarette smoking, hypercholesterolemia and socioeconomic status. The results of this study showed a higher seroprevalence of Helicobacter pylori infection in patients with CAD compared to controls (78.8% versus 58.3%, p < 0.05). However, Helicobacter pylori seropositivity was not associated with coronary artery risk factors (smoking, body mass index, diabetes mellitus, hypertension, total cholesterol and socioeconomic status) either in the whole study population or in the patients and control subjects analyzed separately (P > 0.05). Further study are needed to clarify the precise role of Helicobacter pylori infection on the development of coronary artery disease.

Periodontal microbiota in patients with coronary artery disease measured by real-time polymerase chain reaction: a case-control study.

BACKGROUND: Recent data have shown that periodontal disease may increase the risk of occurrence of coronary heart disease in which inflammation initiated by bacteria and their compounds might be a common causal factor. This case-control study aimed at studying the relationship between periodontal disease and coronary artery disease (CAD) based on clinical and periodontal microbiologic parameters. METHODS: A total of 90 male subjects, 48 to 80 years of age, were included in this study. Forty-five men had CAD (CAD+), which was confirmed by coronary angiography. Forty-five age-matched controls showed no history or symptoms of CAD (CAD-). All subjects underwent a clinical periodontal examination including assessment of tooth loss, probing depth, clinical attachment level, and bleeding on probing. In the CAD+ group, this examination took place 1 day before coronary angiography. Subgingival microbial samples were taken and evaluated by means of real-time polymerase chain reaction (RT-PCR) for the total amount of bacteria and the following periodontopathogens: Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Parvimonas micra (formerly Micromonas micros), Dialister pneumosintes, and Campylobacter rectus. RESULTS: Compared to control subjects, CAD+ subjects had significantly deeper pockets (2.28 mm versus 2.96 mm; P <0.001) and greater attachment loss (2.85 mm versus 3.65 mm; P <0.001), and this difference remained statistically significant after adjusting for smoking. No significant differences were observed between cases and controls with regard to the number of teeth present. P. intermedia was the only periodontal pathogen that showed significantly higher mean counts in CAD+ subjects compared to CAD- subjects. Higher counts of total bacteria, P. micra, D. pneumosintes, and C. rectus were found in the CAD- group. CONCLUSION: The results suggest that a relationship between periodontal disease and coronary heart disease exists, although P. intermedia was the only periodontopathogen related to CAD.

Relationship of periodontal infection to serum antibody levels to periodontopathic bacteria and inflammatory markers in periodontitis patients with coronary heart disease.

Several reports have demonstrated a possible association of periodontal infections with coronary heart disease (CHD) by elevated antibody titre to periodontopathic bacteria in CHD patients compared with non-diseased controls. Although each periodontopathic bacterium may vary in virulence for periodontitis and atherosclerosis, antibody response to multiple bacteria in CHD patients has not been understood fully. Therefore, serum levels of antibody to 12 periodontopathic bacteria together with other atherosclerotic risk markers were compared among 51 patients with CHD, 55 patients with moderate to severe chronic periodontitis and 37 healthy individuals. The antibody response was the most prevalent for Porphyromonas gingivalis, a major causative organism, in CHD as well as periodontitis patients. However, antibody positivity was different between CHD and periodontitis if the response was analysed for two different strains of P. gingivalis, namely FDC381 and Su63. While periodontitis patients were positive for both P. gingivalis FDC381 and Su63, a high frequency of antibody positivity for P. gingivalis Su63 but not for FDC381 was observed in CHD patients. The results indicate that the presence of particular periodontopathic bacteria with high virulence may affect atherogenesis. Identifying the virulence factors of P. gingivalis Su63 may gain insight into the new therapeutic modality for infection-induced deterioration of atherosclerosis.

Socioeconomic status, pathogen burden and cardiovascular disease risk.

OBJECTIVE: Socioeconomic status (SES) is inversely associated with coronary heart disease (CHD) risk. Cumulative pathogen burden may also predict future CHD. The hypothesis was tested that lower SES is associated with a greater pathogen burden, and that pathogen burden accounts in part for SES differences in cardiovascular risk factors. METHODS: This was a cross-sectional observational study involving the clinical examination of 451 men and women aged 51-72 without CHD, recruited from the Whitehall II epidemiological cohort. SES was defined by grade of employment, and pathogen burden by summing positive serostatus for Chlamydia pneumoniae, cytomegalovirus and herpes simplex virus 1. Cardiovascular risk factors were also assessed. RESULTS: Pathogen burden averaged 1.94 (SD) 0.93 in the lower grade group, compared with 1.64 (0.97) and 1.64 (0.93) in the intermediate and higher grade groups (p = 0.011). Pathogen burden was associated with a higher body mass index, waist/hip ratio, blood pressure and incidence of diabetes. There were SES differences in waist/hip ratio, high-density lipoprotein-cholesterol, fasting glucose, glycated haemoglobin, lung function, smoking and diabetes. The SES gradient in these cardiovascular risk factors was unchanged when pathogen burden was taken into account statistically. CONCLUSIONS: Although serological signs of infection with common pathogens are more frequent in lower SES groups, their distribution across the social gradient does not match the linear increases in CHD risk present across higher, intermediate and lower SES groups. Additionally, pathogen burden does not appear to mediate SES differences in cardiovascular risk profiles.

Bacterial profile and burden of periodontal infection in subjects with a diagnosis of acute coronary syndrome.

BACKGROUND: Periodontitis has been identified as a potential risk factor in cardiovascular diseases. It is possible that the stimulation of host responses to oral infections may result in vascular damage and the inducement of blood clotting. The aim of this study was to assess the role of periodontal infection and bacterial burden as an explanatory variable to the activation of the inflammatory process leading to acute coronary syndrome (ACS). METHODS: A total of 161 consecutive surviving cases admitted with a diagnosis of ACS and 161 control subjects, matched with cases according to their gender, socioeconomic level, and smoking status, were studied. Serum white blood cell (WBC) counts, high- and low-density lipoprotein (HDL/LDL) levels, high-sensitivity C-reactive protein (hsC-rp) levels, and clinical periodontal routine parameters were studied. The subgingival pathogens were assayed by the checkerboard DNA-DNA hybridization method. RESULTS: Total oral bacterial load was higher in the subjects with ACS (mean difference: 17.4x10(5); SD: 10.8; 95% confidence interval [CI]: 4.2 to 17.4; P<0.001), and significant for 26 of 40 species including Porphyromonas gingivalis, Tannerella forsythensis, and Treponema denticola. Serum WBC counts, hsC-rp levels, Streptococcus intermedius, and Streptococcus sanguis, were explanatory factors to acute coronary syndrome status (Nagelkerke r2=0.49). CONCLUSION: The oral bacterial load of S. intermedius, S. sanguis, Streptococcus anginosus, T. forsythensis, T. denticola, and P. gingivalis may be concomitant risk factors in the development of ACS.

Seropositivity to Chlamydia pneumoniae or Helicobacter pylori and coronary artery disease.

Our aim was to investigate the relationship between the serologic status concerning Chlamydia pneumoniae and Helicobacter pylori with the presence of coronary artery disease (CAD), which remain a controversial issue in literature. We studied 208 patients with CAD and 94 controls with no evidence of obstructive CAD; all of them angiographically confirmed. The seropositivity to C. pneumoniae was 91% in patients with CAD vs 86% in controls (P>0.05). The H. pylori seroprevalence rates were 77% and 68%, respectively (P>0.05). The multivariate analysis, adjusting for age, sex, educational level, diabetes, hypertension, obesity, smoking, family history of CAD and lipids, confirmed the results of univariate analysis. Therefore, this study adds evidence against the association of seropositivity to C. pneumoniae and H. pylori with angiographically documented CAD.

Chlamydia LPS and MOMP seropositivity are associated with different cytokine profiles in patients with coronary heart disease.

BACKGROUND: Persistent Chlamydia pneumoniae infection within atherosclerotic plaques are possible stimulators of inflammation in atherosclerosis. Why the microbe develops persistency in some individuals is unknown, but experimental studies in cell cultures and animals have demonstrated the levels of gamma interferon (IFNgamma) and interleukin 10 (IL-10) to be of crucial importance. DESIGN: We wanted to evaluate whether Chlamydia seropositivity in patients with coronary heart disease (CHD) (n = 193) was associated with elevated IFNgamma and IL-10. Two methods for detection of Chlamydia antibodies were included as well as analysis of tumour necrosis factor alpha (TNFalpha), soluble vascular cell adhesion molecule 1 (sVCAM-1) and soluble E-selectin for the evaluation of vascular inflammation. RESULTS: We found that patients with IgA antibodies towards Chlamydia lipopolysaccharide (LPS) had elevated levels of IFNgamma (P = 0.048), IL-10 (P = 0.029), TNFalpha (P = 0.009) and sE-selectin (P = 0.045), while Chlamydia LPS IgG seropositivity predicted elevated levels of IL-10 (P = 0.013). Patients with IgA antibodies towards C. pneumoniae major outer membrane protein (MOMP) without simultaneous LPS IgA seropositivity had lower levels of IFNgamma and sVCAM-1 when compared to patients with Chlamydia LPS IgA alone (P = 0.005 for IFNgamma, P = 0.016 for VCAM-1) and patients with combined Chlamydia MOMP and LPS IgA seropositivity (P = 0.046 and P = 0.013, respectively). CONCLUSIONS: In summary, we demonstrated an association between Chlamydia LPS IgA seropositivity and elevated levels of IFNgamma, IL-10, TNFalpha, sVCAM-1 and sE-selectin in CHD patients that might indicate persistent Chlamydia infection and a proinflammatory state. On the other hand, C. pneumoniae MOMP antibodies were not associated with elevated inflammatory markers and might merely be indicative of past infection, possibly with successful microbe clearance.

Ectasia and severe atherosclerosis: relationships with chlamydia pneumoniae, helicobacterpylori, and inflammatory markers.

To date, there has been no convincing evidence for an association between Chlamydia pneumoniae or Helicobacter pylori and ectasia. In this case-control study, we have investigated the association of H. pylori and C. pneumoniae seropositivity with ectasia, severe coronary atherosclerosis, and normal vessels, which were so classified by coronary angiography. We have also evaluated the influence of these infections on inflammatory markers such as high-sensitive C-reactive protein (hsCRP) and interleukin 6 (IL-6). Of the 796 patients undergoing coronary angiography for suspected ischemic heart disease, 244 patients were recruited. Of these, 91 had normal vessels, 88 had 3 or more obstructed vessels, and 65 had ectatic vessels without atherosclerosis. Eighty-seven atherosclerotic patients (98.9%) were positive for C. pneumoniae IgG, as were 64 ectatic patients (98.5%) and 76 controls (83.5%) (P < 0.001). Forty-two atherosclerotic patients (47.7%) were positive for C. pneumoniae IgM, as were 43 ectatic patients (66.2%) and 43 controls (47.3%) (P = 0.036). Seventy-two atherosclerotic patients (81.8%) were positive for H. pylori IgA, as were 26 ectatic patients (40.0%) and 44 controls (48.4%) (P < 0.001). High-sensitive CRP levels were significantly higher in ectatic patients (5.639 mg/L) than in controls (4.390 mg/L) (P = 0.032), and IL-6 levels were significantly higher in atherosclerotic patients (33.92 U/L) than in controls (14.01 U/L) (P < 0.001). Interleukin-6 levels were higher in H. pylori seropositive patients, and hsCRP levels were higher in C. pneumoniae seropositive patients, when compared with seronegatives. We suggest that, as in atherosclerosis, C. pneumoniae infection is related to ectasia, with raised CRP levels.

Effect of clarithromycin treatment on Chlamydia pneumoniae in vascular tissue of patients with coronary artery disease: a randomized, double-blind, placebo-controlled trial.

Several small clinical trials have indicated that antibiotic treatment of Chlamydia pneumoniae infection is associated with a better outcome in patients with coronary artery disease (CAD). It has not been demonstrated whether antibiotic treatment eradicates C. pneumoniae from vascular tissue. The aim of the present study was to assess the effect of clarithromycin on the presence of C. pneumoniae in the vascular tissue of patients with CAD. Patients who had CAD and who were waiting for coronary artery bypass graft surgery were enrolled in a randomized, double-blind, placebo-controlled trial. Patients were treated with clarithromycin at 500 mg or placebo once daily from the day of inclusion in the study until surgery. Several vascular tissue specimens were obtained during surgery. The presence of C. pneumoniae in vascular tissue specimens was examined by immunohistochemical staining (IHC) and two PCR assays. Chlamydia immunoglobulin G (IgG) titers were determined by an enzyme-linked immunosorbent assay at the time of inclusion in the study and 8 weeks after surgery. A total of 76 patients were included, and 180 vascular tissue specimens were obtained (80 specimens from the group treated with clarithromycin and 100 specimens from the group treated with placebo). Thirty-five patients received clarithromycin (mean duration, 27 days; standard deviation [SD], 12.2 days), and 41 patients received placebo (mean duration, 27 days; SD, 13.9 days). IHC detected the C. pneumoniae major outer membrane protein antigen in 73.8% of the specimens from the group treated with clarithromycin and 77.0% of the specimens from the group treated with placebo (P was not significant). Chlamydia lipopolysaccharide antigen was found in only one specimen from the group that received placebo. C. pneumoniae DNA was not detected in any specimen. Baseline Chlamydia-specific IgG titers were equally distributed in both groups and were not significantly different after treatment. There was no indication of an active C. pneumoniae infection in vascular tissue. Chlamydia-specific IgG titers remained unchanged throughout the study in both the antibiotic- and the placebo-treated patients.

The impact of Helicobacter pylori infection on coronary heart disease in a Korean population.

BACKGROUND/AIMS: Although several studies have claimed that Helicobacter pylori (H. pylori) infection is related to cardiovascular disease, it is still uncertain whether it is related to the acute process or the chronic inflammatory atherosclerotic changes. The aim of our study was to confirm the impact of active H. pylori infection on coronary heart disease, acute inflammatory factors, and the coagulation factors. METHODS: A total of 94 patients completed questionnaires about occupation, smoking, past medical history, and socio-economic status. The serum of the subjects was drawn for a low density lipoprotein test, white blood cell count, C reactive protein, fibrinogen, homocysteine, prothrombin time, activated partial thrombin time, plasminogen activator inhibitor type-1, and tissue-type plasminogen test. All of the subjects underwent a coronary angiography and an upper gastrointestinal endoscopy for the diagnosis of coronary heart disease and H. pylori infection, respectively. RESULTS: There was no significant difference in acute inflammatory factors, coagulation factors, atheromatous burden score, and Jeopardy score between the H. pylori-infected group and non-infected group. Odds ratio of H. pylori infection on coronary heart disease was 2.59 (95% CI, 0.80-6.17), but it diminished below 1.0 (95% CI, 0.14-1.36) after adjusting for conventional risk factors such as age, gender, diabetes, hypertension, smoking, body mass index and socio-economic status. CONCLUSIONS: H. pylori infection is not an independent risk factor for coronary heart disease, and it does not alter the coagulation system or evoke the systemic inflammatory response.

Histopathologic signs for the inflammatory role of Chlamydia pneumoniae in the high-grade atherosclerotic coronary artery wall.

The aim of the study was to prove the long-lasting and continuously harmful effect of chronic Chlamydia pneumoniae (CPn) infection on vessel walls in patients with diffuse coronary artery disease (CAD). In surgically obtained endarterectomized atherosclerotic plaques grade VI-VIII (Stary classification) from 10 patients with diffuse coronary artery disease and chronic (7) or past (3) CPn infection, signs of inflammatory response of the vessel wall on infectious agents were studied. In all 10 endarterectomized plaque step serial sections, immunologic signs of vessel wall response were present (positive T- and B-lymphocytes, macrophages, and capillarogenesis). In 8 of 10 patients' atherosclerotic plaque, unique features of active vasculitis in the neoarteriolar wall as well as arteriologenesis, were found. Seven of these 8 patients had serologically proven chronic CPn infection, and 1 had past infection. Features of vasculitis as well as arteriologenesis were absent in 2 patients who recovered from CPn infection at the time of surgery. In the endarterectomized segments of 3 randomly chosen patients in this study, the polymerase chain reaction method revealed positive DNA of CPn. Two of these patients had chronic infection, but the third had only a past CPn infection. This study provides evidence that CPn infection has continuous and a long-lasting inflammatory response in the high-grade atherosclerotic coronary artery vessel wall.

Hemochromatosis and the enigma of misplaced iron: implications for infectious disease and survival.

The mystery surrounding the apparent lack of iron within the macrophages of individuals with hereditary hemochromatosis, a condition of excessive uptake of dietary iron, has yet to be fully explained. We have suggested that iron deficiency of macrophages in people with hereditary hemochromatosis mutations is associated with increased resistance to infection by Yersinia and other intracellular pathogens, a selection pressure resulting in unusually high current population frequencies of hereditary hemochromatosis mutations. Such selection pressure has been called Epidemic Pathogenic Selection (EPS). In support of the theory of EPS, a considerable number of virulent species of bacteria multiply mainly in iron-rich macrophages of their mammalian hosts. Among these fastidious pathogens are strains of Chlamydia, Coxiella, Francisella, Legionella, Mycobacterium, Salmonella and Yersinia. Iron deficiency of macrophages of persons with hereditary hemochromatosis gene mutations may result in increased resistance to members of these bacterial pathogens. People with genes that result in hereditary hemochromatosis may be protected against coronary artery disease associated with Chlamydia and Coxiella infection in the absence of iron overload. In the clinical setting, when a patient appears to be iron deficient, the reason for this should be carefully evaluated. Iron supplementation may adversely affect the health of individuals who have mounted an acute phase response to infection, injury or stress, or who carry genes predisposing them to iron overload disorders.

Serological evidence of Helicobacter pylori infection in UK South Asian and European populations: implications for gastric cancer and coronary heart disease.

OBJECTIVES: To describe the prevalence of serological evidence of infection with Helicobacter pylori among people of South Asian and European ethnic origins and to assess its association with prevalent coronary heart disease (CHD). METHODS: We used a quantitative method to compare IgG antibodies to H. pylori in a population sample of 300 South Asians and 302 Europeans in Newcastle upon Tyne, UK. RESULTS: For men and women, respectively, H. pylori IgG (95% confidence interval) was 16.7 microg/ml (13.9, 20.2) and 11.3 (9.4, 13.5) among Europeans and 11.6 (9.8, 13.7) and 14.3 (12.1, 16.9) among South Asians. Levels were higher in older participants and in those of lower socioeconomic status. The ratio of geometric mean IgG, (95% confidence interval) adjusted for age, sex and socioeconomic status, in those with and without CHD was 1.02 (0.49, 2.11) among Europeans and 1.79 (1.01, 3.17) among South Asians. Antibodies against staphylococcal enterotoxins A and B were higher among South Asians than Europeans. CONCLUSIONS: The prevalence of H. pylori infection among UK South Asians does not reflect that of their countries of origin, nor their lower prevalence of gastric cancer. The association with CHD in South Asians requires corroboration in other studies.